Abstract

Amyloid-β (Aβ) aggregates are a hallmark of Alzheimer’s disease (AD). Through the misfolding process of Aβ in the brain, oligomeric forms of Aβ accumulate and significantly damage the brain cells inducing neuronal loss and cognitive dysfunctions that lead to AD. We hypothesized that decrease in Aβ oligomers during the aggregation process might be able to reduce Aβ-dependent brain damage. As taurine-like chemicals are often reported to have direct binding abilities to Aβ, we prepared a chemical library that consisted of taurine-carbohydrate derivatives to search for molecules that target Aβ and accelerate its fibrillogenesis. Here, we report that 1-deoxy-1-(2-sulfoethylamino)-D-fructose stimulates the formation of relatively less toxic Aβ fibrils leading to prevention of cognitive deficits in AD acute model mice.

abstract = "Amyloid-β (Aβ) aggregates are a hallmark of Alzheimer{\textquoteright}s disease (AD). Through the misfolding process of Aβ in the brain, oligomeric forms of Aβ accumulate and significantly damage the brain cells inducing neuronal loss and cognitive dysfunctions that lead to AD. We hypothesized that decrease in Aβ oligomers during the aggregation process might be able to reduce Aβ-dependent brain damage. As taurine-like chemicals are often reported to have direct binding abilities to Aβ, we prepared a chemical library that consisted of taurine-carbohydrate derivatives to search for molecules that target Aβ and accelerate its fibrillogenesis. Here, we report that 1-deoxy-1-(2-sulfoethylamino)-D-fructose stimulates the formation of relatively less toxic Aβ fibrils leading to prevention of cognitive deficits in AD acute model mice.",

N2 - Amyloid-β (Aβ) aggregates are a hallmark of Alzheimer’s disease (AD). Through the misfolding process of Aβ in the brain, oligomeric forms of Aβ accumulate and significantly damage the brain cells inducing neuronal loss and cognitive dysfunctions that lead to AD. We hypothesized that decrease in Aβ oligomers during the aggregation process might be able to reduce Aβ-dependent brain damage. As taurine-like chemicals are often reported to have direct binding abilities to Aβ, we prepared a chemical library that consisted of taurine-carbohydrate derivatives to search for molecules that target Aβ and accelerate its fibrillogenesis. Here, we report that 1-deoxy-1-(2-sulfoethylamino)-D-fructose stimulates the formation of relatively less toxic Aβ fibrils leading to prevention of cognitive deficits in AD acute model mice.

AB - Amyloid-β (Aβ) aggregates are a hallmark of Alzheimer’s disease (AD). Through the misfolding process of Aβ in the brain, oligomeric forms of Aβ accumulate and significantly damage the brain cells inducing neuronal loss and cognitive dysfunctions that lead to AD. We hypothesized that decrease in Aβ oligomers during the aggregation process might be able to reduce Aβ-dependent brain damage. As taurine-like chemicals are often reported to have direct binding abilities to Aβ, we prepared a chemical library that consisted of taurine-carbohydrate derivatives to search for molecules that target Aβ and accelerate its fibrillogenesis. Here, we report that 1-deoxy-1-(2-sulfoethylamino)-D-fructose stimulates the formation of relatively less toxic Aβ fibrils leading to prevention of cognitive deficits in AD acute model mice.